Related Experiment Video
Updated: Jan 3, 2026
Live-Cell Imaging Assays to Study Glioblastoma Brain Tumor Stem Cell Migration and Invasion
Published on: August 29, 2018
LQB‑118 compound inhibits migration and induces cell death in glioblastoma cells
Paula Sabbo Bernardo1, Gustavo Henrique C Guimarães1, Fernanda Costas C De Faria1
1Laboratory of Cellular and Molecular Hemato‑Oncology, Program of Molecular Hemato‑Oncology, Brazilian National Cancer Institute (INCA), Rio de Janeiro, RJ 20230‑130, Brazil.
Abstract:
Glioblastoma (GBM) is the most frequent malignant brain tumor. It represents the most aggressive astrocytoma with an overall survival of 14 months. Despite improvements in surgery techniques, radio‑ and chemotherapy, most patients present treatment resistance, recurrence and disease progression. Therefore, development of effective alternative therapies is essential to overcome treatment failure. The purpose of the study was to evaluate the antitumoral activity of the synthetic compound LQB‑118, in vitro. Monolayer and three‑dimensional (3D) cell culture systems of human‑derived GBM cell lines were used to evaluate the effect of LQB‑118 on cell viability, cell death and migration. LQB‑118 reduced cell viability as determined by MTT and trypan blue exclusion assays and promoted apoptosis in monolayer cell lines with an intrinsic temozolomide (TMZ)‑resistance profile. In 3D culture models, LQB‑118 reduced cell viability as evaluated by APH assay and inhibited cell migration while the TMZ resistance profile was maintained. Moreover, LQB‑118 reduced p38 and AKT expression and phosphorylation, whereas it reduced only the phosphorylated ERK1/2 form. LQB‑118 reduced p38 and NRF2 expression, an axis that is associated with TMZ resistance, revealing a mechanism to overcome resistance. LQB‑118 also demonstrated an additional effect when combined with ionizing radiation and cisplatin. In conclusion, the present data demonstrated that LQB‑118 maintained its effectiveness in a 3D cell conformation, which shares more similarities with the tumor mass. LQB‑118 is a promising agent for GBM treatment as monotherapy and associated with radiotherapy or cisplatin. Its effect is associated with inhibition of GBM‑related survival signaling pathways.
Insights
The synthetic compound LQB-118 shows significant antitumoral activity against glioblastoma (GBM) cells, even those resistant to temozolomide (TMZ). This compound effectively reduces cell viability and migration, offering a promising new therapeutic avenue for GBM treatment.
Area of Science:
- Neuro-oncology
- Cancer Biology
- Drug Discovery
Background:
- Glioblastoma (GBM) is an aggressive brain tumor with poor prognosis.
- Current treatments face challenges due to drug resistance, recurrence, and disease progression.
- Novel therapeutic strategies are crucial to improve patient outcomes.
Purpose of the Study:
- To evaluate the in vitro antitumoral activity of the synthetic compound LQB-118 against human-derived glioblastoma (GBM) cell lines.
- To assess LQB-118's effects on cell viability, cell death, and migration in both monolayer and 3D culture models.
- To investigate the molecular mechanisms underlying LQB-118's efficacy, particularly in overcoming temozolomide (TMZ) resistance.
Main Methods:
- Utilized monolayer and three-dimensional (3D) cell culture systems of human GBM cell lines.
- Assessed cell viability using MTT and trypan blue exclusion assays, and APH assay for 3D models.
- Analyzed apoptosis, cell migration, and expression/phosphorylation of key signaling proteins (p38, AKT, ERK1/2, NRF2).
Main Results:
- LQB-118 reduced GBM cell viability and induced apoptosis in temozolomide (TMZ)-resistant cell lines.
- In 3D models, LQB-118 inhibited cell viability and migration, maintaining efficacy against TMZ-resistant cells.
- LQB-118 modulated signaling pathways (p38, AKT, ERK1/2, NRF2), including the p38/NRF2 axis linked to TMZ resistance.
- LQB-118 showed synergistic effects when combined with ionizing radiation and cisplatin.
Conclusions:
- LQB-118 demonstrates potent antitumoral activity in vitro, including in 3D models that mimic tumor structure.
- The compound effectively targets GBM cells, including those with intrinsic TMZ resistance.
- LQB-118's mechanism involves inhibiting key GBM survival pathways.
- LQB-118 is a promising candidate for GBM treatment, as monotherapy or in combination with standard therapies like radiotherapy and cisplatin.
